Catalogue Number: T9161-19-USB
| Manufacturer: | United States Biological |
| Physical state: | Supplied as a liquid in PBS, 1% BSA, 0.02% sodium azide. Labeled with fluorescein isothiocyanate (FITC). |
| Type: | Monoclonal Primary Antibody - Conjugated |
| Shipping Condition: | Blue Ice |
| Unit(s): | 100 ug |
| Host name: | Rat |
| Clone: | 9G293 (HM104) |
| Isotype: | IgG2a |
| Immunogen: | Recombinant protein corresponding to the extracellular part of the TNF-receptor I |
| Application: | FC, IP, IHC, FLISA |
Description: TNF-RI (~55-60 kD) is present on most cell types and is considered to play a prominent role in cell stimulation by TNF-alpha. TNF-alpha activates inflammatory responses, induces apoptosis, regulates cellular proliferation, and may even promote cancer progression. The effects of TNF-alpha are mediated by TNF-R1 and TNF-R2, which have both distinct and overlapping downstream signaling cascades. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-R1 is equally well activated by both the 17 kDa soluble and 26 kDa membrane-bound form, whereas TNF-R2 is efficiently activated only by the membrane bound form of TNF-alpha. TNF-R1 signaling is initiated when trimeric TNF-alpha binds TNF-R1 receptors. Subsequent TNF-R1 trimerization promotes the recruitment of a proximal signaling complex composed of TNF Receptor Associated protein with a Death Domain (TRADD), Receptor Interacting Protein (RIP), cellular Inhibitor of Apoptosis Protein 1 (cIAP1), TNF Receptor Associated Factor 2 (TRAF2), and likely TRAF5. Studies with TNF-R1-deficient mice indicate that TNF-R1 mediates most of the proliferation, pro-inflammatory, and apoptosis-activating pathways.
FOR RESEARCH USE ONLY
Recognizes the extracellular part and the soluble receptor of the mouse TUMOR NECROSIS FACTOR RECEPTOR I. Reactivity with soluble TNF-Receptor is inhibited by high conentrations of both mouse and human TNF-alpha.
Protein G purified
Monoclonal